Nervous Control Of Heart Rate Research Articles

Respiratory sinus arrhythmia and the heart rate response to carotid baroreceptor activation after hard dynamic exercise in humans

The aim of this study was to examine the influence of 20 min of hard exercise (HR >160 beats min −1) on the efficacy of the cardiac parasympathetic nervous control of heart rate in humans (20–31 years; of either sex). This intensity of exercise was chosen to produce strong activation of the cardiac sympathetic nerves. Using well-controlled stimulus parameters, the efficacy of cardiac parasympathetic control of heart rate was assessed by recording the heart rate response to carotid baroreceptor activation (CBR) and the amplitude of respiratory sinus arrhythmia (RSA). Measurements were made while the subject performed light exercise (100–135 beats min −1) before (Control 1) and after very brief (Control 2) and prolonged (20 min; post) periods of hard exercise. There was no difference in the CBR in the three different measurement periods; 0.33±0.17, 0.38±0.18 and 0.39±0.18 beats min −1 mm Hg −1 (mean±S.D., N=6) for Control 1, Control 2 and post, respectively. At a heart rate of 120 beats min −1, amplitude of the RSA was 6.1±2.4, 5.6±2.4 and 3.3±2.1 beats min −1 for Control 1, Control 2 and post, respectively ( P<0.001 post vs. Control 1 and Control 2, N=8). The decrease in RSA amplitude following hard exercise may be attributable to an exercise-induced reduction in airway resistance and work of breathing. Overall, these results do not support the hypothesis that sustained hard exercise that produces strong activation of cardiac sympathetic nerves reduces cardiac parasympathetic efficacy.

The neuranatomical basis of central control of cardiorespiratory interactions in vertebrates.

The neuranatomical basis of central control of cardiorespiratory interactions in vertebrates.

Alterations in autonomic nervous control of heart rate among tourists at 2700 and 3700 m above sea level

Many travelers who are not specially trained for activities at high altitude are at risk of physical problems, including cardiovascular disorders, when exposed to high-altitude environments. In the present study, we investigated how actual acute exposure to altitudes of 2700 and 3700 m affected the autonomic nervous control of heart rate in untrained office workers. Physiological parameters (heart rate, respiratory rate, arterial blood oxygen saturation, and end-expiratory carbon dioxide tension) were measured at sea level, 2700 m, and 3700 m. The power of heart rate variability was quantified by determining the areas of the spectrum in 2 component widths: low frequency (LF; 0.04-0.15 Hz) and high frequency (HF; 0.15-0.5 Hz). The ratio of LF power to HF power (LF:HF), which is considered to be an index of cardiac sympathetic tone, was also assessed. Both HF and LF heart rate variability decreased according to the elevation of altitude. High- and low-frequency powers at 3700 m were significantly lower than those at sea level (P < .01 for HF, P < .05 for LF). The LF:HF ratio at 2700 m was not significantly different from that at sea level. However, it was significantly increased at 3700 m (P < .01). At 2700 and 3700 m, the activity of the autonomic nervous system measured by heart rate variability was decreased in untrained office workers. The sympathetic nervous system was dominant to the parasympathetic at 3700 m. These alterations in the autonomic nervous system might play some role in physical fitness at high altitudes.

The autonomic nervous control of heart rate in ducks during voluntary diving.

Autonomic nervous control of heart rate was studied in voluntarily diving ducks (Aythya affinis). Ducks were injected with the muscarinic blocker atropine, the beta-adrenergic blocker nadolol, the beta-adrenergic agonist isoproterenol, and a combination of both atropine and nadolol. Saline injection was used as a control treatment. The reduction in heart rate (from the predive level) normally seen during a dive was abolished by atropine. Nadolol reduced heart rate during all phases of diving activity-predive, dive, and postdive-indicating that sympathetic output to the heart was not withdrawn during diving. Isoproterenol increased heart rate before, during, and after the dive, although the proportional increase in heart rate was not as high during the dive as compared with the increase in routine heart rate or heart rate during the predive or postdive phase. The parasympathetic system predominates in the control of heart rate during diving despite the maintenance of efferent sympathetic influences to the heart, perhaps due to accentuated antagonism between the two branches of the autonomic nervous system.

Autonomic nervous control of heart rate orienting and alpha responses in dog.

The object of this experiment is to study the autonomic nervous control of alpha responses elicited in classical conditioning. Twenty-two mongrel dogs were trained in classical discriminative conditioning. Typical two-phase tachycardic responses were observed in positive (CS+) trials while only the earliest, phase 1, response was observed in negative (CS-) trials. The phase 1 response, which was identical in CS+ and CS-trials, was compared in dogs before and after selective SA-nodal parasympathectomy (N = 7) and beta-adrenergic blockade (N = 11). The phase 1 tachycardic response was eliminated by selective SA-nodal parasympathectomy but not by beta-adrenergic blockade. We conclude that the phase 1 response observed in both CS+ and CS-trials with similar time sequence and magnitude is an alpha response. The heart rate orienting response results from a withdrawal of parasympathetic activity with little or no change in sympathetic tone.

Autonomic nervous control of heart rate in muskrats during exercise in air and under water.

Neural control of the cardiac responses to exercise in air (running) and under water (diving) was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine and the beta-adrenergic blocker nadolol. Saline injection was used as a control. Controls running on a treadmill showed a marked increase in heart rate with exercise. Atropine-treated animals had a higher resting heart rate than controls, but heart rate still increased with running. Nadolol-treated animals had a lower resting heart rate than controls and displayed a less pronounced increase in heart rate with running than controls. Animals treated with a combination of atropine and nadolol had a resting heart rate similar to that of controls but their heart rate was unaffected by running. Thus, exercise tachycardia in muskrats is due to activation of the sympathetic system and also to a reduction in parasympathetic tone. Heart rate decreased markedly during voluntary submergence in controls but rose as muskrats swam submerged against increasing water flows. Nevertheless, diving bradycardia was still present. Free-diving bradycardia and the relative increase in heart rate with underwater exercise were abolished by atropine and unaffected by nadolol. Hence, unlike the cardiac response to exercise in air, the cardiac response to underwater exercise is due only to a reduction in parasympathetic tone. Injection of the beta-adrenergic agonist isoproterenol markedly increased heart rate in air but had little effect during voluntary and forced dives, indicating a marked decrease in the sensitivity of cardiac cells to adrenergic stimulation during submergence. These results strongly suggest that accentuated antagonism between the two branches of the autonomic nervous system occurs during diving so that parasympathetic influences on the heart predominate and inhibit any chronotropic response to adrenergic stimulation.

Autonomic nervous control of heart rate during blood-flow restricted exercise in man.

Power spectra of instantaneous heart rate (fc) allows the estimation of the contribution of sympathetic and parasympathetic control of fc during steady-state conditions. The present study was designed to examine autonomic control of fc as influenced by normal dynamic leg exercise and by ischemic leg exercise. Eight subjects performed supine cycle ergometry at 30% of their control peak work rate, with and without blood-flow restriction. Blood-flow restriction was induced by exposing the exercising legs to a supra-atmospheric pressure of 6.7 kPa (leg positive pressure; LPP). The exercise responses of arterial pressure and fc increased (P < 0.05) by LPP exposure. The exaggerated pressor response may be attributed to a chemoreflex drive originating in the ischemic muscles. Exposure to LPP during exercise also produced a significant decrease in parasympathetically mediated high frequency (HF; 0.15-1.00 Hz) fluctuation of fc, as indicated by a decrease (P < 0.05) in percent HF power compared to the control exercise level. During LPP exercise, the sympathetically mediated very low frequency (VLF; 0-0.05 Hz) fluctuation of fc increased, as indicated by an increase (P < 0.05) in percent VLF power above control exercise levels. Both LPP and control exercise conditions decreased (P < 0.05) power in all frequency ranges of interest compared to their respective resting conditions. The results suggest that the increase in fc associated with normal dynamic exercise was mediated predominantly by parasympathetic withdrawal, whereas the exaggerated fc response during ischemic exercise resulted from a combination of cardiac sympathetic drive and parasympathetic withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of quinpirole on autonomic nervous control of heart rate in rats.

The effects of quinpirole, a specific dopamine DA2 receptor agonist, on autonomic nervous control of heart rate, were studied in normotensive pithed rats, by analysing its action on the tachycardia and bradycardia evoked by electrical stimulation of the cardioaccelerator (10 V; 1 ms; 0.5, 1, 3, 6 Hz) and vagus (10 V; 1 ms; 3, 6, 9 Hz) nerves respectively. Quinpirole (10-50-100 micrograms kg-1 iv) reduced the cardioacceleration elicited by electrical stimulation but not that by noradrenaline (3 micrograms kg-1 iv). The effect on electrical stimulation was blocked by domperidone (0.5 mg kg-1 iv) but not by SCH 23390 (0.2 mg kg-1 iv) or idazoxan (0.3 mg kg-1 iv). At 1, 5, 10, 30 micrograms kg-1 iv, quinpirole decreased vagal but not acetylcholine-induced bradycardia. The effect on electrical stimulation was inhibited by domperidone (0.5 mg kg-1 iv) but not by SCH 23390 (0.2 mg kg-1 iv), prazosin (0.1 mg kg-1 iv) or idazoxan (0.3 mg kg-1 iv). The data point to the presence of presynaptic and/or ganglionic dopamine receptors in the sympathetic and parasympathetic innervation of the rat heart, where stimulation inhibits the release of neuromediators.

Sympathetic and parasympathetic influence on blood pressure and heart rate variability in Wistar-Kyoto and spontaneously hypertensive rats.

The relative influence of sympathetic and parasympathetic nervous control of heart rate and heart rate variability, of mean arterial pressure (MAP) and MAP variability was investigated in young spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). An on-line computerized system was used for continuous intra-arterial measurements of MAP and heart rate every 2.5 min in freely moving rats with indwelling arterial catheters. Variability was expressed as the standard deviation in each rat. Heart rate and MAP showed clear diurnal rhythms, both in WKY and SHR. Blood pressure variability was clearly higher in SHR than in WKY, both during dark active hours and during light hours of relative sleep, and it did not change in response to either beta-adrenoceptor or vagal blockade. Structural vascular changes with the consequent increase in vascular reactivity may be one explanation for the elevated blood pressure variability in SHR. Heart rate variability was clearly reduced in SHR compared with WKY. This may be due to a reduced tonic vagal discharge in SHR, whereby a vagally mediated tachycardia is eliminated. The vagal withdrawal is part of the defence reaction, which is more easily elicited in SHR than in WKY.

Autonomic nervous control of heart rate: sympathetic-parasympathetic interactions and age related differences.

A factorial experimental design was used to quantify the changes in heart rate produced by stimulation of the cardiac sympathetic and vagal nerves in eleven adult dogs and four puppies, and to quantify the extent of the peripheral sympathetic-vagal interactions. The chronotropic responses to autonomic stimulation were significantly less in the puppies than in the adult dogs, which suggests that autonomic regulation is functionally incomplete in the puppies. In both adult dogs and puppies, the chronotropic responses to autonomic nerve stimulation were bilaterally asymmetrical. The heart rate responses to a given level of right-sided stimulation of either the sympathetic or vagal nerves were greater than those to comparable left-sided stimulation. In both adult dogs and puppies, there were significant sympathetic-vagal interactions, such that the sympathetic enhancement of heart rate was less effective the higher the background level of vagal activity. The sympathetic-vagal interactions were prominent in the puppies as well as in the adult animals, regardless of whether the stimulated sympathetic and vagal nerves were located ipsilaterally or contralaterally to one another. Thus, the mechanisms responsible for the sympathetic-vagal interactions appear to be fully developed in puppies. Also, the cardiac sympathetic nerve endings that originate from one side of the body must lie in close apposition to the cardiac vagal nerve endings that originate from either the same side or from the opposite side of the body.

Nervous control of heart rate: activity in the cardiac vagus of the dogfish.

In the absence of any sympathetic innervation to the heart, nervous control of heart rate in the dogfish is solely attributable to inhibitory parasympathetic input from the vagus nerve. Action potentials can be recorded from the cardiac vagus of the dogfish following its exposure in the anterior cardinal sinus. The rates of heartbeat and ventilation, blood pressure, hematocrit, and responses to external stimuli such as hypoxia, which include a bradycardia, remained typical of fish with their nervous and circulatory systems virtually intact. The recordings included sporadically active units that accelerated during hypoxia, possibly inducing the bradycardia, and regular bursts of action potentials synchronous with ventilatory movements that appeared to arise reflexly from stimulation of pharyngeal proprioceptors. These bursts may loosely couple the respiratory and cardiac pumps, increasing the probability of concurrence between periods of maximum water and blood flow. The preparation enables detailed study of the temporal relationships between the pumps and its neurophysiological basis.

Age-dependent pattern of autonomic heart rate control during hypoxia in fetal and newborn lambs.

Autonomic nervous control of heart rate (HR) during hypoxia was studied longitudinally using 9 chronically catheterized fetal lambs (109 day to term) and 10 newborn lambs (2--28 days old). Changes in heart rate (deltaHR) during hypoxia were age-dependent. Before 120 days of gestation deltaHR was insignificant, but between 120 days to term bradycardia occurred. The newborn response was marked tachycardia. Autonomic influences on HR were quantified using atropine and propranolol blockade. In fetal lambs, antagonistic increases in parasympathetic and sympathetic outflows were evident during hypoxia. In hypoxic lambs 120 days to term, net bradycardia reflected predominant parasympathetic cardio-deceleration; before 120 days of gestation both the parasympathetic and sympathetic outflows increased, but no net deltaHR occurred. In hypoxic newborn lambs, sympathetic and parasympathetic changes contributed synergistically to the net tachycardia. Thus the pattern of autonomic control of HR during hypoxia differs in fetal and newborn lambs. Changes in sympathetic and parasympathetic influences are antagonistic in the fetus, but synergistic in the newborn.

Quantitative computer analysis of cardiac and respiratory activity in newborn infants.

ArticleQuantitative computer analysis of cardiac and respiratory activity in newborn infants.P A Tarlo, I Välimäki, and P M RautaharjuP A Tarlo, I Välimäki, and P M RautaharjuPublished Online:01 Jul 1971https://doi.org/10.1152/jappl.1971.31.1.70MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByCurrent definitions for neonatal apnoea: Are they evidence based?28 May 2013 | Journal of Paediatrics and Child Health, Vol. 49, No. 9Surfactant replacement partially restores the activity of pulmonary stretch receptors in surfactant-depleted catsRichard Sindelar, Anders Jonzon, Andreas Schulze, and Gunnar Sedin1 February 2006 | Journal of Applied Physiology, Vol. 100, No. 2Spectral Analysis of Heart Rate and Blood Pressure VariabilityClinics in Perinatology, Vol. 26, No. 4Elevated arterial blood pressure is associated with peri-intraventricular haemorrhageEuropean Journal of Pediatrics, Vol. 153, No. 112 Quantification of fetal heart rate variation using a probability distribution matrixBaillière's Clinical Obstetrics and Gynaecology, Vol. 8, No. 3Continuous monitoring of heart rate variability in preterm infantsEarly Human Development, Vol. 37, No. 2Changes in autonomic cardiovascular control in mid-pregnancyClinical Physiology, Vol. 12, No. 5Effects of glycopyrrolate and atropine on heart rate variabilityActa Anaesthesiologica Scandinavica, Vol. 35, No. 5Heart rate variability in infants subsequently suffering sudden infant death syndrome (SIDS)Early Human Development, Vol. 22, No. 2Vincristine treatment of acute lymphoblastic leukemia induces transient autonomic cardioneuropathyCancer, Vol. 64, No. 4Heart rate variation in normal infants and victims of the sudden infant death syndromeEarly Human Development, Vol. 19, No. 3Multivariate autoregressive modeling of autonomic cardiovascular control in neonatal lambComputers and Biomedical Research, Vol. 21, No. 6Heart-Rate Variability and SIDS Examination of Heart-Rate Patterns Using an Expert System GeneratorAnnals of the New York Academy of Sciences, Vol. 533, No. 1 The Sudden InTranscutaneous PO2, PCO2 and heart rate patterns during normal postnatal adaptation and respiratory distressEarly Human Development, Vol. 16, No. 1Detection of components of autonomic cardiac control by time series analysis of heart rate in lambs: technical reportEffects of haemodialysis on heart rate variability in chronic renal failure8 July 2009 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 46, No. 7Reactivity of autonomic nervous control of heart rate in diabetes mellitus and juvenile rheumatoid arthritis8 July 2009 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 46, No. 8Analysis of neonatal heart rate variability by a microprocessor-based on-line systemJournal of Perinatal Medicine, Vol. 13, No. 5Perinatal heart rate variability and circulatory adaptation in association with normal labor and after elective cesarean sectionAmerican Journal of Obstetrics and Gynecology, Vol. 147, No. 8Impact of thermal vasomotor control on the heart rate variability of newborn infantsEarly Human Development, Vol. 8, No. 1Analysis of heart rate and beat-to-beat variability: Interval difference indexAmerican Journal of Obstetrics and Gynecology, Vol. 138, No. 3Heart rate variability in full-term normal and abnormal newborn infants during sleepBrain and Development, Vol. 1, No. 1Quantitative Characterization of Heart Rate During Exercise8 July 2009 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 39, No. sup153Quantification of fetal heart rate variability by magnetocardiography and direct electrocardiographyAmerican Journal of Obstetrics and Gynecology, Vol. 128, No. 5REFERENCESActa Paediatrica, Vol. 63, No. s250 More from this issue > Volume 31Issue 1July 1971Pages 70-5 https://doi.org/10.1152/jappl.1971.31.1.70PubMed5556965History Published online 1 July 1971 Published in print 1 July 1971 Metrics

Nervous control of heart rate during excitement in the adult White Leghorn cock.

Nervous control of heart rate during excitement in the adult White Leghorn cock.

Some nonlinear control techniques novel to control engineers employed by a biological control system

The nervous control of heart rate in man was studied through dynamic analysis of experimental results and computer simulation. The heart rate changes caused by respiration were found to be accurately analyzable and predictable, as related by a fifth-order nonlinear differential equation which proved to have specific physiological meaning. The nonlinear characteristics of the equations are interesting in that they also show how neural controls can produce certain dynamic characteristics not normally encountered in control engineering practice. This paper is to be published in the Proceedings of the First IFAC Moscow Congress by Butterworth Scientific Publications in 1960.